Hepatic nitrosative stress in experimental diabetes
Copyright policy )Hepatic nitrosative stress in experimental diabetes
The effects of the inhibition of nitrosative stress by aminoguanidine in an experimental model of diabetes mellitus (DM) were investigated.Twenty-one male Wistar rats were divided into three groups: control (CO), diabetic (DM), and diabetic treated with aminoguanidine (DM+AG). Aminoguanidine (aminoguanidine hemisulfate salt, Sigma Chemical Co., St. Louis, MO, USA) was used at a dose of 50 mg/kg (i.p.) during the last 30 days of the experiment. The expression levels of liver lipoperoxidation (TBARS - nmol/mg protein), inducible oxide nitric synthase (iNOS), nitrotyrosine and the NFκB nuclear transcription factor p65 were examined using western blot analysis.The DM group demonstrated an increase in lipoperoxidation and in the expression of iNOS, nitrotyrosine and p65. Aminoguanidine reduced hepatic lipid peroxidation and protein expression levels of iNOS, nitrotyrosine and p65.Aminoguanidine treatment reduces liver oxidative and nitrosative stress in diabetic animals. In addition, aminoguanidine reduced the expression of p65 in the liver.
Male, Transcription Factor RelA, Down-Regulation, Nitric Oxide Synthase Type II, Guanidines, Reactive Nitrogen Species, Diabetes Mellitus, Experimental, Rats, Oxidative Stress, Liver, Animals, Tyrosine, Lipid Peroxidation, Enzyme Inhibitors, Nitric Oxide Synthase, Rats, Wistar, Reactive Oxygen Species
Male, Transcription Factor RelA, Down-Regulation, Nitric Oxide Synthase Type II, Guanidines, Reactive Nitrogen Species, Diabetes Mellitus, Experimental, Rats, Oxidative Stress, Liver, Animals, Tyrosine, Lipid Peroxidation, Enzyme Inhibitors, Nitric Oxide Synthase, Rats, Wistar, Reactive Oxygen Species
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